Eaten carbohydrates from glucidic foods (bread, pasta, potatoes, fruit, sugar . . . ) are transformed into glucose in the intestine during digestion. Glucose passes the intestinal wall and goes into the bloodstream. This provokes glycemia peaks; increases in blood glucose levels which during fasting are approximately 1 g per liter of blood. Insulin is the hormone responsible for lowering blood glucose levels during the course of the metabolic processes following digestion. Increased glycemia during the postprandial period triggers insulin secretion by the pancreas, which induces glucose storage by the body organs, especially liver and muscle. This reverses glycemia to its fasting levels.
In a healthy individual, insulin secretion is proportional to blood glucose levels. The insulin secreted by his pancreas is thus that required to lower glycemia. In some people, insulin response is out of proportion with regards to glycemia.
However, in some individuals, the body tissues do not respond properly to insulin. Insulin receptors in the tissues cease to function adequately and gluco-dependant cells fail to recognize the presence of insulin. As a result, the pancreas needs to secrete more insulin to help glucose enter these cells. The pancreas tries to keep up with this increased demand for insulin by producing more. This phenomenon is called insulin resistance (also known as low insulin sensitivity). Many people with insulin resistance have high levels of both glucose and insulin circulating in their blood at the same time. Eventually, the pancreas fails to keep up with the body's need for insulin, leading to Type II diabetes.
Insulin resistance and Type II diabetes are associated to increased risk of heart attacks, strokes, amputation, diabetic retinopathy, and kidney failure. For extreme cases, circulation of limbs is affected, potentially requiring amputation. Loss of hearing, eyesight, and cognitive ability has also been linked to these conditions
According to the World Health Organization, at least 171 million people worldwide suffered from type II diabetes. Its incidence is increasing rapidly, and it is estimated that by 2030, this number will almost double. Insulin resistance is an even more frequent condition, which affected up to 40% adults in the US in 2000. Insulin resistance has been traditionally considered a condition of the middle-old age. However, its prevalence has been dramatically increasing in the pediatric population during the last decades.
A specific case of insulin resistance is the gestational diabetes. Today, 3-10% of pregnancies are affected by abnormal glucose regulation and control.
Infants who were born to mothers with gestational diabetes are at a higher risk than other infants to develop complications. The two main risks these mothers impose on the baby are growth abnormalities and chemical imbalances after birth, which may require admission to a neonatal intensive care unit. Infants who were born to said mothers are at risk of being both large for gestational age (macrosomic) and small for gestational age. Macrosomia in turn increases the risk of instrumental deliveries (e.g. forceps, ventouse and caesarean section) or problems during vaginal delivery (such as shoulder dystocia). Neonates are also at an increased risk of low blood glucose (hypoglycemia), jaundice, high red blood cell mass (polycythemia), low blood calcium (hypocalcemia) and magnesium (hypomagnesemia). Gestational diabetes also interferes with maturation, causing dysmature babies prone to respiratory distress syndrome due to incomplete lung maturation and impaired surfactant synthesis.
Management of insulin resistance in children and adults is essentially based on dietary and lifestyle changes, including healthier dietary habits and increased exercise. These practices can be very efficient in improving insulin sensitivity and in slowing the progression of the disease, but they are difficult to apply and actually not followed by most patients. Type II diabetes can be treated with drugs promoting insulin sensitivity, but their efficacy in reducing the rate of progression of the disease is quite low. Insulin treatment is required during the most advanced phases of the disease.
Some infants, in particular those who were born preterm and/or who experienced intra-uterine growth retardation (IUGR), present a high risk of insulin resistance. Approximately 40% of low-gestation newborns of birthweight less than 1250 g develop hyperglycaemia during the weeks that follow birth. The hyperglycaemia in these newborns is due, in part, to hepatic and peripheral insulin resistance.
Hyperglycaemia in these infants can result in tissular damage. The most common intervention to deal with hyperglycaemia is to decrease the glucose load provided to the infant. This, together with the impaired glucose uptake due to low insulin sensitivity, results in an inadequate energy supply to the infant tissues, which can lead to poor growth and increased risk of complications.
Products containing n-3 polyunsaturated fatty acids, fibers, oligosaccharides and even probiotics have been proposed as nutritional solutions to improve insulin sensitivity and to reduce insulin resistance. However, the efficacy of these nutritional interventions is quite marginal and even controversial, with studies showing no or even deleterious effects.
Thus, there is a need to provide an effective, safe and compliable nutritional solution to improve insulin resistance in infants who were born preterm and/or who experienced IUGR, in pregnant women suffering from gestational diabetes and in children, adolescents, and adults suffering from insulin resistance and/or type II diabetes.
There is also a need for this nutritional intervention in young mammals, in particular infants and children, preferably infants, but also young pets.